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Biomedical subjects

L L Porter

Publications and source records attributed to L L Porter.

32 records · Page 2Linked to original sources
PubMed1987

Long-lasting potentiation of synaptic potentials in the motor cortex produced by stimulation of the sensory cortex in the cat: a basis of motor learning.

A long-lasting increase in the efficiency of synaptic transmission in the central nervous system has been thought to be one of the bases of learning and memory. To explore the possibility that the motor cortex (area 4 gamma) itself is involved in motor learning, the existence of long-term potentiation (LTP) was examined by recording excitatory postsynaptic potentials (EPSPs) from motor cortical neurons. Short tetanic intracortical microstimulation (ICMS) of the somatic sensory cortex produced a marked potentiation of the EPSPs in a small group of motor cortical neurons. The results raised the possibility that the input from the sensory cortex participates in motor learning and retention of the learned motor skills.

Animals↗
PubMed1986

Synaptic connections of callosal projection neurons in the vibrissal region of mouse primary motor cortex: an electron microscopic/horseradish peroxidase study.

Reciprocal axonal projections between homotypic areas of the vibrissal region of mouse primary motor cortex (MsI) (Porter and White: Neurosci. Lett. 47:37-40, '84) suggested the existence of reciprocal synaptic connections between callosal projection neurons and callosal afferents. In the present study, the retrograde transport of horseradish peroxidase (HRP) was combined with lesion-induced degeneration to identify synapses between callosal afferents and callosal neurons in the corresponding region of the contralateral cortex. The procedure was as follows: MsI was injected with HRP and aspirated on the following day. After 4 days, the animals were perfused and motor cortex was processed for HRP according to a variation of the Adams (Brain Res. 176:33-47,'77) technique, and postfixed in OsO4. The methods used consistently filled fine dendritic branches and spines with dense reaction product, thus allowing examination of synaptic contacts with these processes. All callosal projection neurons were identified as pyramidal neurons, having somata in cortical layers II/III and V. Labeled cells from each of the two levels were prepared for electron microscopy, and that part of each cell's apical dendrite that traversed the superficial cortical layers, where most callosal axons terminate, was cut in an unbroken series of thin sections. Micrographs were taken of all labeled profiles in each thin section, and tracings of the profiles were assembled to reconstruct the apical dendrites. Data on the distribution, type, and amount of callosal and other synapses with the shaft and spines of the apical dendrites were obtained by examining the reconstructions. In addition, profiles of basal dendrites of layer II/III cells were examined in thin sections to ascertain the numbers of callosal and other synapses formed with their shafts and spines. The proportion of synapses that each dendrite formed with callosal axon terminals was compared to the concentration of callosal afferents in the neuropil. Dendrites of both layer II/III and layer V pyramidal cells synapsed with callosal axon terminals. The apical and basal dendrites of layer II/III neurons formed a similar proportion of their synapses with callosal afferents, and this was similar to the concentration of callosal synapses in the surrounding neuropil. Segments of apical dendrites belonging to layer V and layer II/III neurons course through neuropil containing nearly the same concentration of degenerating callosal terminals, but the layer V cells form fewer callosal synapses.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Acute nonlymphocytic leukemia after treatment of small cell lung cancer.

From 1977 to 1982, 377 patients with small cell lung cancer were treated at Vanderbilt University Medical Center. All patients received combination chemotherapy consisting of cyclophosphamide, doxorubicin, and vincristine (CAV) with or without methotrexate, etoposide, and/or hexamethylmelamine. Thoracic and/or prophylactic cranial irradiation was administered to 159 (42 percent) and 192 (51 percent) patients, respectively. Acute nonlymphocytic leukemia was observed in two patients at 22 and 81 months from the start of therapy. The relative risk of leukemia was 154 (95 percent confidence limit, 38 to 293). A Kaplan-Meier estimate of the cumulative probability of leukemia was 1.9 +/- 1.4 percent seven years after the start of treatment. The relative risk of leukemia is significantly increased in this group of patients (p less than 0.0001). Acute nonlymphocytic leukemia is a long-term complication of small cell lung cancer therapy.

Adult↗
PubMed1986

High-dose pilot studies in extensive-stage small-cell lung cancer.

Small-cell lung cancer is rarely cured with standard chemotherapy, despite initial good responses. The concept of high-dose induction therapy for extensive-stage patients has been explained in a series of pilot studies. The rationale of this approach and the most recent preliminary results will be presented.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Combination chemotherapy with vindesine, etoposide, and cisplatin in non-small cell lung cancer: a pilot study of the Southeastern Cancer Study Group.

Ninety-two patients with advanced non-small cell lung cancer were treated with a combination chemotherapy regimen containing cisplatin, vindesine, and etoposide. Eighteen patients (20%) achieved major responses to therapy (three complete responders and 15 partial responders). Response rates were similar in each histologic subtype. Initial performance status was an important determinant of response; 42% of the patients with a Karnofsky performance status greater than or equal to 70% responded versus 5% of those with a performance status less than 50%. The median duration of partial response was 21 weeks; complete responders had a median response duration of 50 weeks. The median survival for the entire group was 23.5 weeks. Toxicity with this regimen was acceptable; myelosuppression was the major toxic effect and was severe in only 10% of the patients. This regimen produced response rates comparable to those reported with other combinations containing cisplatin. Survival advantage in patients receiving this treatment is not established.

Adenocarcinoma↗
PubMed1985

Extensive-stage small-cell bronchogenic carcinoma: intensive induction chemotherapy with high-dose cyclophosphamide plus high-dose etoposide.

Seventeen ambulatory patients with extensive-stage small-cell lung cancer received one or two courses of high-dose induction chemotherapy consisting of cyclophosphamide (100 mg/kg) plus etopside (1,200 mg/m2) followed by four or five cycles of conventional-dose cyclophosphamide (1,000 mg/m2), doxorubicin (40 mg/m2), and vincristine (1.4 mg/m2) (CAV) given every 21 days. No additional chemotherapy was given until relapse or progression was documented. Response was assessed initially after high-dose induction therapy and again after completion of all chemotherapy. After induction therapy, 16/17 (94%) patients had achieved an objective response, including five (29%) complete responses and 11 (65%) partial responses. Two partially responding patients improved to a complete response after CAV, while one partial responder progressed and one patient died of an intercurrent illness while receiving CAV. Thus, the overall response after completing all chemotherapy was 15/16 (94%), including seven (44%) complete responses and eight (50%) partial responses. Median response duration was six months (range, 3 to 11 months), and overall median survival was ten months (range, 2 to 17 months). All 31 courses of induction therapy were associated with leukopenia (less than 1,000/microL), 81% with thrombocytopenia (less than 20,000/microL), and 77% with fever (greater than 38.5 degrees C). Seven episodes of bacteremia and one axillary abscess were documented, and there was one treatment-related death (6%). These toxicities are similar to that produced by high-dose etoposide alone. High-dose cyclophosphamide combined with high-dose etoposide can be administered to ambulatory patients with extensive-stage small-cell lung cancer without requiring bone marrow transplantation to reestablish hematopoiesis. Complete response and median survival rates, however, are similar to those obtained with less intensive therapy.

Adult↗
PubMed1985

High-dose etoposide (VP-16) in small-cell lung cancer.

Etoposide (VP-16) is one of the most active drugs against small-cell lung cancer. There may be a steep dose-response relationship, and we have explored the use of etoposide as a single agent in a high dose (1,200 mg/m2) without bone marrow transplantation, for patients with very bulky, extensive-stage disease. This therapy is well tolerated in patients having good performance status, with myelosuppression representing the major toxicity. Our data suggest there may truly be a steep dose-response relationship. We have continued to explore intensive induction therapy for selected very poor-prognosis patients by adding high-dose cyclophosphamide (100 mg/kg) to high-dose etoposide. This combination is also very myelotoxic, but quite similar to etoposide alone. Our current study adds cisplatin (120 mg/m2) to the high-dose cyclophosphamide-etoposide schedule in an attempt to take advantage of the synergism seen with these drugs in various other circumstances. This series of studies will give us information regarding the feasibility of intensive induction therapy and provide data for the design of phase III studies.

Adult↗
PubMed1985

Cisplatin and etoposide combination chemotherapy for refractory small cell carcinoma of the lung.

Twenty-nine patients with refractory recurrent small cell carcinoma of the lung were treated with cisplatin (40 mg/m2) and etoposide (200 mg/m2) each day for 3 days, repeated every 3-4 weeks. Fifteen of these patients had received etoposide in their original treatment regimen. Fifteen (52%) of all patients had a major response, as did nine (60%) of the patients with prior exposure to etoposide. Myelotoxicity was moderately severe. The median duration of responses was 3 months (range, 6-36 weeks). This study suggests synergism between cisplatin and etoposide. The toxicity seen in this heavily pretreated group of patients suggests that smaller doses be studied in this group. The synergism may be best utilized in the initial regimens against small cell lung cancer.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1984

Termination of callosal afferents onto identified callosal projection neurons in the primary motor cortex of the mouse.

Techniques utilizing the retrograde transport of horseradish peroxidase and lesion-induced degeneration have been used to identify neurons which form the callosal projection pathway and callosal axon terminals in the primary motor cortex of the mouse. Synapses occur between callosal projection neurons and degenerating callosal afferents, demonstrating a direct synaptic link between neurons which project to homotopic regions of the contralateral cortex.

Animals↗
PubMed1983

Afferent and efferent pathways of the vibrissal region of primary motor cortex in the mouse.

The afferent and efferent connections of the vibrissal representation within the mouse primary motor cortex (MsI) were identified by using the retrograde transport of horseradish peroxidase (HRP) and the anterograde transport of tritiated amino acids injected into MsI. Following aldehyde perfusion brains were frozen-sectioned at 40 microns and reacted for HRP using the 3-3' diaminobenzidine-cobalt chloride technique of Adams ('77). Alternate HRP reacted sections were processed for autoradiography. HRP-filled pyramidal cell somata and concentrations of developed silver grains above background levels were observed in both the vibrissal area of primary somatosensory cortex (SmI) cortex (i.e., the posteromedial barrel subfield; PMBSF cortex) and in the face region of SmII (area 40). In both regions labeled somata occurred predominantly in cortical layers II-III and V. Autoradiographic label was superimposed over the regions containing labeled somata but exhibited a less distinct laminar organization. A dense reciprocal projection connected the injection site with the homotopic area in contralateral MsI; somata occurred for the most part in layers III and V. Developed silver grains were uniformly dispersed over the area containing labeled cell bodies. HRP-labeled pyramidal somata were noted in contralateral PMBSF cortex, but no silver grains occurred in this region. Reciprocal projections linked MsI cortex with the ipsilateral thalamic nuclei: ventralis pars lateralis (VL) and centralis pars lateralis (CL) and with the zona incerta (ZI). Labeled cell bodies and developed silver grains were more dense in VL than in CL. The ipsilateral striatum and thalamic reticular nucleus (NRT) received afferents from the motor cortex but did not project to it. Thus, the vibrissal area of primary motor cortex is connected with a number of cortical and subcortical structures, each of which has been shown to play a role in motor performance. Identification of the afferent and efferent pathways of MsI cortex will now enable further investigation of the ultrastructural and synaptic organization of the vibrissal area of MsI.

Afferent Pathways↗
PubMed1979

Mycotic aneurysms of the hepatic artery. Treatment with arterial embolization.

In a 29 year old white man with acute Staphylococcus aureus endocarditis of the aortic valve two mycotic aneurysms of the hepatic artery developed during antibiotic treatment. One aneurysm was treated with surgical ligation and the other with Gelfoam embolization. Successful obliteration of the embolized aneurysm was demonstrated by hepatic arteriography two months later. The pathogenesis, clinical manifestations and management of hepatic mycotic aneurysms is discussed with emphasis on arterial embolization.

Adult↗
PubMedDate not supplied

Oral dolasetron mesylate in patients receiving moderately emetogenic platinum-containing chemotherapy. Oral Dolasetron Dose Response Study Group.

PURPOSE: This double-blind, dose-response study was conducted to assess the safety and efficacy of four oral doses of dolasetron mesylate for preventing acute emesis in cancer patients receiving their first course of moderately emetogenic platinum-containing chemotherapy. PATIENTS AND METHODS: Patients were randomized to receive a single oral dose of 25, 50, 100, or 200 mg dolasetron 30 minutes before receiving IV carboplatin (275-400 mg/m2)- or cisplatin (20-50 mg/m2)-containing chemotherapy, then monitored for nausea and vomiting for 24 hours. RESULTS: Three hundred seven cancer patients from 32 sites completed the study. There was a statistically significant dose response across the four doses for complete response (no emetic episodes or rescue medication): 44.7%, 71.3%, 73.2%, and 82.5% for the 25, 50, 100, or 200 mg doses of dolasetron, respectively. Patients' nausea severity and patient satisfaction visual analogue scale scores also showed a statistically significant trend with dose. All doses of dolasetron were well tolerated. The most common adverse events were headache (17.6%) and dizziness (2.0%). DISCUSSION: This study demonstrates the safety and antiemetic efficacy of oral dolasetron mesylate in patients receiving moderately emetogenic platinum-containing chemotherapy with the highest antiemetic activity observed at 200 mg.

Administration, Oral↗